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Biomedical subjects

R W Hill

Publications and source records attributed to R W Hill.

At least 19 recordsLinked to original sources
PubMed1990

Characterization of clones of HIV-1 infected HuT 78 cells defective in gag gene processing and of SIV clones producing large amounts of envelope glycoprotein.

Single-cell clones of HIV-1 (FRE-3) or SIV/Mne infected HuT 78 cells were obtained by plating dilutions of virally infected HuT 78 cells on a monolayer of sheep choroid plexus cells in 96-well microtiter plates. Several of these clones produce HIV-1 virus mutants that accumulate the gag precursor polyprotein and lack a functional protease. These protease-deficient viruses are non-infectious and consist of aberrant "immature" virus particles as determined by electron microscopy. Several SIV mutants are also described that produce large amounts of either the envelope glycoprotein gp120 or the nucleic acid binding gag protein. These mutants are useful for the purification of these retroviral proteins, in developing assays of protease inhibitors, and in preparing SIV envelope protein vaccines.

Animals↗
PubMed1989

Molecular characterization and comparison of simian immunodeficiency virus isolates from macaques, mangabeys, and African green monkeys.

Simian immunodeficiency virus (SIV)/Mne has been inoculated into three species of macaques and into baboons. Virus was isolated from all the macaques who subsequently died at 15 to 120 weeks (mean 80 weeks) with various manifestations of immune deficiency. Individual animals varied in their viral antibody profile as a function of time after infection. Independent SIV isolates obtained from African green monkeys and magabeys were compared to SIV/Mne for their ability to replicate in lymphocytes and macrophages and with respect to the immunological relatedness of their viral proteins. Antibodies present in human immunodeficiency virus-2 (HIV-2)-infected individuals were readily detected by the virus produced by a single-cell clone of SIV/Mne.

Animals↗
PubMed1988

Suppression of growth of 7,12-dimethylbenzanthracene-induced mammary carcinomas in female rats by repeated whole-body hyperthermia (41-42 degrees C).

The purpose of this study was to examine effects of repeated whole-body hyperthermia on the growth of carcinogen-induced rat mammary carcinomas. Female Sprague-Dawley rats were treated intragastrically with a single dose (100 mg/kg) of the carcinogen 7,12-dimethylbenzanthracene (DMBA) at 2 months of age. Subsequently, when each rat had a minimum of one palpable mammary carcinoma, the animals were divided into two groups, one to receive hyperthermia treatments and the other to serve as controls. The hyperthermia-treated rats received 14-20 1-hour episodes of whole-body hyperthermia (averaging 41.4 degrees C, colonic) over a period of 3-4 weeks. The animals were anesthetized with sodium pentabarbital during these treatments to suppress their thermoregulation and to minimize stress mediated by higher brain functions. Their temperature was raised by exposure to high air temperatures. Control rats were anesthetized on the same schedule, and with the same doses of barbital, as hyperthermia-treated rats, but during anesthetization were placed at lower air temperatures such that their body temperatures remained normal. Tumor volumes were measured once per week. By the end of the first week, hyperthermia had suppressed carcinoma growth: whereas 78% of control carcinomas had increased in volume, 73% of hyperthermia-treated ones had decreased in volume. The average volume of mammary carcinomas in hyperthermia-treated rats after 1 week was significantly smaller than the average volume of mammary carcinomas in control rats: 0.34 vs. 0.66 cm3 (effects of differences in initial volume statistically removed). This difference had enlarged by the end of four weeks to 0.11 cm3 (hyperthermia-treated) vs. 0.80 cm3 (control). Overall, this study provides compelling evidence that whole-body hyperthermia in the range of 41-42 degrees C suppresses growth of DM-BA-induced rat mammary carcinomas, and it describes a technique for hyperthermia induction in which stresses specific to hyperthermia are minimized or avoided.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1988

Inoculation of baboons and macaques with simian immunodeficiency virus/Mne, a primate lentivirus closely related to human immunodeficiency virus type 2.

A primate lymphotropic lentivirus was isolated on the human T-cell line HuT 78 after cocultivation of a lymph node from a pig-tailed macaque (Macaca nemestrina) that had died with malignant lymphoma. This isolate, originally designated M. nemestrina immunodeficiency virus (MnIV) and now classified as simian immunodeficiency virus (SIV/Mne), was inoculated intravenously into three juvenile rhesus monkeys (Macaca mulatta), three juvenile pig-tailed macaques (M. nemestrina), and two juvenile baboons (Papio cynocephalus). All six macaques became viremic by 3 weeks after inoculation, whereas neither of the baboons developed viremia. One pig-tailed macaque died at 15 weeks with suppurative peritonitis secondary to ulcerative, necrotizing colitis. Immunologic abnormalities included a marked decrease in CD4+ peripheral blood lymphocytes. Although five macaques mounted an antibody response to SIV/Mne, the animal that died at 15 weeks remained antibody negative. Three other macaques (two rhesus and one pig-tailed) died 66 to 87 weeks after inoculation after exhibiting progressive weight loss, anemia, and diarrhea. Histopathologic findings at necropsy included various manifestations of immune deficiency, nephropathy, subacute encephalitis, pancreatitis, adenocarcinoma, and lymphoid atrophy. SIV/Mne could be readily isolated from the spleens and lymph nodes of all necropsied macaques, and from the cerebrospinal fluid, brains, bone marrow, livers, and pancreas of some of the animals. SIV antigens were localized by avidin-biotin immunohistochemistry to pancreatic islet cells and to bone marrow endothelial cells. The data suggest that African baboons may be resistant to infection by SIV/Mne, whereas Asian macaques are susceptible to infection with this pathogenic primate lentivirus.

Acquired Immunodeficiency Syndrome↗
PubMed1987

4 modalities of periodontal treatment compared over 5 years.

The purpose of the present study was to assess in a clinical trial over 5 years the results following 4 different modalities of periodontal therapy (pocket elimination or reduction surgery, modified Widman flap surgery, subgingival curettage, and scaling and rool planing). 90 patients were treated. The treatment methods were applied on a random basis to each of the 4 quadrants of the dentition. The patients were given professional tooth cleaning and oral hygiene instructions every 3 months. Pocket depth and attachment levels were scored once a year. 72 patients completed the 5 years of observation. Both patient means for pocket depth and attachment level as well as % distribution of sites with loss of attachment greater than or equal to 2 mm and greater than or equal to 3 mm were compared. For 1-3 mm probing depth, scaling and root planing, as well as subgingival curettage led to significantly less attachment loss than pocket elimination and modified Widman flap surgery. For 4-6 mm pockets, scaling and root planing and curettage had better attachment results than pocket elimination surgery. For the 7-12 mm pockets, there was no statistically significant difference among the results following the various procedures.

Clinical Trials as Topic↗
PubMed1977

Radiographs in periodontics.

Intraoral radiographs are widely used in periodontal diagnosis and research. However, accurate radiographic interpretation is only possible with high quality images. Some of the technical and geometric variables to consider have been presented. Early periodontal lesions are not detected in radiographs. The amount of periodontal destruction in more advanced disease is generally underestimated. The accurate topography of periodontal pockets and the buccal and lingual aspects of the teeth cannot be visualized. Clinical probing is therefore a prerequisite for a complete periodontal diagnosis. However, radiographs are a valuable adjunct for the periodontal diagnosis and the diagnosis of trauma from occlusion. With standardized systems, radiographs may furnish additional quantitative data in clinical research.

Bone Resorption↗
PubMed1976

Jackrabbit ears: surface temperatures and vascular responses.

Blood flow to the ear pinnae is curtailed at ambient temperatures of between 1.4 degrees and 24 degrees C, which minimizes heat loss across the pinnae and allows the surfaces of erect pinnae to approach ambient temperature. The pinnae are warmed by steady or pulsatile vasodilation in some animals when the ambient temperature is between 1 degree and 9 degrees C below body temperature, a response favoring heat loss. When ambient temperature exceeds body temperature by 4 degrees to 5 degrees C, the pinnae are circulated with blood cooler than ambient temperature; this response favors heat influx.

Animals↗
PubMed1976

Prevention of spontaneous leukemia in AKR mice by type-specific immunosuppression of endogenous ecotropic virogenes.

AKR/J mice, 80-90% of which ordinarily die of spontaneous lymphocytic leukemias by 12 months of age, were significantly protected from developing leukemia in the initial experiment by a single course of treatment with AKR serotype-specific antibodies mad in goats and processed as immune gamma globulin (IgG). In experiment 1, IgG was given on the day of birth and on four additional days, and finished on day 14. This schedule resulted in suppression of over 4 logarithms of normal virogene expressions up to 25 days of age and led to partial viral suppression for over 200 days of age. At 365 days of age, 20 of 24 (83.3%) control animals were dead of leukemia whereas six of 30 (20%) treated animals had died of leukemia. In a second experiment, only four inoculations of IgG were given from birth to 20 days, after which they were given three inoculations of radiation-killed vaccine specific for AKR-Gross leukemia virus and one injection of murine sarcoma virus-Gross leukemia virus 10 days later. This combined immunization procedure provided significant virus suppression up to 288 days of age. At 300 days of age, 30 of the 50 (60%) controls had died of leukemia while only 1 of 24 (4.2%) of the immunized mice developed fatal leukemia; the significance of protection for each of the experiments was P LESS THAN 0.001. We conclude that these data establish in classical fashion with type-specific immunosuppression the determining role of type-C endogenous virogenes in leukemogenesis and, at the same time, also established the feasibility of nearly total prevention of leukemia in AKR mice.

AKR murine leukemia virus↗